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Updated: Jul 13, 2026
09:41
Performing and Processing FNA of Anterior Fat Pad for Amyloid
Published on: October 30, 2010
Secondary amyloidosis due to FMF
1Department of Gastroenterology, Hacettepe University Faculty of Medicine, Ankara, Turkey.
Hepato-Gastroenterology
|July 17, 2007
Summary
Familial Mediterranean fever (FMF) is an inherited autoinflammatory disorder. Colchicine prevents attacks and amyloidosis, but alternative treatments are needed for resistant cases.
Area of Science:
- Genetics
- Immunology
- Rheumatology
Background:
- Familial Mediterranean fever (FMF) is an autosomal recessive autoinflammatory disease.
- Characterized by recurrent fever, abdominal, chest, and joint pain.
- Primarily affects Mediterranean populations, with onset typically by age 20.
Purpose of the Study:
- To review the epidemiology and pathophysiology of FMF.
- To highlight secondary (AA) amyloidosis as a severe complication.
- To discuss current treatment limitations and future research directions.
Main Methods:
- Literature review of FMF and AA amyloidosis.
- Analysis of epidemiological and genetic data.
- Discussion of colchicine efficacy and resistance.
Main Results:
- FMF is ethnically restricted, with significant morbidity from AA amyloidosis, particularly nephropathic.
- Colchicine is effective in preventing FMF attacks and amyloidosis.
- No established alternative treatments exist for colchicine-resistant FMF.
Conclusions:
- Further collaborative research is needed to understand FMF-amyloidosis links.
- Development of alternative therapies for resistant FMF is crucial.
- Gathering population-based epidemiological and genetic data is essential.
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Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
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Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...